Airway

HPI: 8 year old Male with PMH of Sickle Cell Disease (HbSC), Post-opt Day 10 for laparoscopic splenectomy for recurrent sequestration crises presents to the Emergency Department (ED) complaining of abdominal pain x 2 days. The pain is described as diffuse and worse in the RUQ. Denies exacerbating or relieving factors. Pain is associated with constipation; last Bowel movement was 7 days prior. Mother states he did have one small BM shortly after surgery. He is tolerating PO without difficulty and does report flatus. She has been giving him Oxycodone 2mg every 6 hours for pain with minimal relief. Upon review of systems, patient reports feeling hot for the past 2 days but without a recorded temperature at home. Additionally, patient complained of a non-productive cough for 2 days and has been “breathing fast” for the same duration of time.

Physical Exam:

BP 112/74 HR 129 RR 24 SpO2 93% on RA Temp 99.9F 26.3 kg

Constitutional: Well developed, well-nourished child who is awake, alert and in moderate distress due to pain and feeling hot; making tears

HEENT: NCAT, pupils PERRLA, neck supple

Respiratory: CTA B/L, no wheezing, rales or rhonchi

Chest/Axilla: Normal symmetrical motion, no tenderness

Cardiac: +S1/S2, RRR, no MRG,

Abdomen: Scars noted over splenectomy site which are clean dry and intact, healing well without discharge; Diminished Bowel Sounds in all quadrants; soft, non-distended with mild tenderness in all 4 quadrants. No rebound or guarding.

Neuro exam: AAO x 3. No deficits

Extremities: no edema, no tenderness or swelling

Pertinent Labs:

CBC: 42.1

HBG: 12.5

HCT: 36.9

Platelets: 721

Seg: 79

Lymphs: 9

Mono: 12

Reticulocyte count: reported as normal

Pertinent Imaging and other tests:

Working Diagnosis:

Generalized abdominal pains

Elevated WBC

Abscess of spleen

ED/Hospital course:

Surgery was consulted in the ED and they believed the pain was not related to the surgery. Abdominal U/S performed at their request showed “s/p splenectomy with gallbladder sludge.” Patient had moderate improvement in his pain after Toradol 15mg IV and Morphine 2mg IV were given in the ED. Patient also received Rocephin 75mg/kg and NS 500mL IV Fluid bolus for presumed infection with the leukocytosis of 42.1.

The patient was admitted to Pediatric Step down for further evaluation and management. Overnight, he remained comfortable with stable vital signs, afebrile and saturating 94-96% on 2L NC. On Hospital day #1, patient became febrile to 103F and continued to deny chest pain, SOB or difficulty breathing. The cough remained unchanged since admission. A repeat Chest X-Ray was obtained and the patient was diagnosed with Acute Chest Syndrome and received exchange transfusion the same day (Refer to Image below) Additionally, he received Ceftriaxone, Azithromycin, Nitric oxide and IVF at ¾ maintenance ate throughout hospitalization. On Hospital Day #4 he was discharged home.

Pearls:

Acute Chest Syndrome

It is the leading cause of death in patients with SCD in the United States

Most often occurs as a single episode, but patients may have multiple attacks resulting in chronic lung disease

Pearl’s from Wed conference August 2nd 2017:

-All that wheezes is not asthma (or COPD).
-Use diagnostics to rule out mimics such as pneumonia or ptx.
-Get the CXR in COPD exacerbation, not routinely in simple asthma exacerbation.
-Good evidence and NNT’s for benefit of ipratropium, systemic steroids, magnesium, and BiPAP.
-Intubation last resort for asthma. Remember to adjust I to E ratio on vent.
-Steroids at discharge for asthma/COPD. Antibiotics at discharge for COPD.
-Discharge with a plan! (and a spacer)

Dr. Patel: Sepsis Core Measures

-Sepsis core measures are from CMS, not from SSC guidelines or Sepsis 3.0. They are not necessarily rooted in great evidence, but we have to follow them!
-Remember the 3 and 6 hour severe sepsis and septic shock bundles. Timing is based on presentation time (when chart displays severe sepsis, septic shock), not door time. To make your life easy, just use door time to meet the metrics.
-The focused exam for septic shock can now just be documented with one statement, which is in Medhost. Make sure to click that.
-Fluids from the field count (as your 30 cc/kg), as long as it is given as a bolus and documented on the chart.
-Antibiotic choice and timing both looked at for core measures. For choice, best to go with a monotherapy agent first to meet the metric.

Dr. Patel: Pulmonary Cases

-The term HCAP is not in the newest pneumonia guidelines from 2016.
-Treat HCAP like CAP unless the patient is going to the MICU. If going to the MICU, cover for MRSA and Pseudomonas.

Hemoptysis:

-Minor hemoptysis (streaks in the sputum)–d/c unless CXR abnormal
-Moderate hemoptysis (frank hemoptysis)—admit for further work up and obs
-Massive hemoptysis (hemoptysis interfering with respirations)–intubate and consult pulmonary (for bronch) and IR (for possible bronchial artery embolization). If there is a suspicion of a bronchovesicular fistula or other arterial fistula, CT surgery may also need to be on board.

Medical Student Pearls

One of our current medical student’s Mike Taylor put together some info on questions that were raised in conference:

Intentional “L Main Bronchus Intubation:” (for hemoptysis)

Take Home Points from 1995 Anesthesiology Case Report:
-Can use a double lumen ET tube with a endobronchial cuff
-The inflated endobronchial cuff can tamponade the hemorrhaging R lung and occlude airflow into it. This allows only the L lung to be effectively intubated and the provider not have to be tasked with putting the tube in the L main bronchus
Reference: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1949905

Take home points from 2012 Retrospective Cohort Study:
-With normal white counts, pts with bandemia of at least 11% had higher in hospital mortality
-So 11% or higher could use as a cut off for admission, more aggressive treatment, etc.
Reference: https://www.ncbi.nlm.nih.gov/pubmed/22939096

Special thanks to Chief Dan Poor PGY-4 for organizing this week’s Conference Pearls and for Mike Taylor MS-IV for his Medical Student Pearls

You head over to bed 44 to meet the BLS crew as they start telling you about an 82 year old man who has been having trouble breathing and is “confused” as per his family. His oxygen saturation when you check is 76% and quicker than you can say “sepsis”, the eager resident has popped the grey airway box open and is setting up to intubate.

You slap the NRB on and turn the O2 up all the way. So why is the resident so focused on finding and placing a nasal cannula too?!

Apneic oxygenation (AO) is used to extend the time until critical arterial desaturation (SaO2 88-90%) following cessation of breathing/ventilation that occurs during intubation. AO, similar to our other RSI preparation, premedication, and positioning, is used to optimize the patient prior to the first intubation attempt.

First demonstrated by anesthesiologists over 50 years ago, the alveoli of the lungs will continue to take up oxygen even in the absence of active breathing. AO focuses on increasing a patient’s oxygen saturation through “nitrogen washout” in first the alveoli, and then throughout the circulation. This effectively replaces the nitrogen one inhales in normal atmospheric air with oxygen and increases the patient’s overall oxygen storage in both the lungs (95% of a person’s natural reservoir) and bloodstream. Maximizing pre-oxygenation provides us an additional buffer of time for “safe apnea” during oral intubation. In a 2011 article in the Annals of Emergency Medicine, Weingart et aloutline recommendations to reduce the risk of hypoxemia during emergency tracheal intubations which include emphasis on:

Take home: Keep in mind the acronym “NO DESAT” which stands for “Nasal Oxygen During Efforts Securing ATube”. A nasal cannula with high flow rates should be placed on every patient prior to endotracheal intubation and left in place during attempts in order to reduce the risk of hypoxemia and deterioration.

In comes a 34-year-old male who is obtunded with pinpoint pupils and breathing at five times a minute; likely due to heroin abuse. He wakes up after Narcan is appropriately administered, but now he wants to leave. What is the risk of death if he leaves? Do we restrain him against his will to monitor him for possible recurrent respiratory depression?

We have some pre-hospital literature that looked into this issue. The studies looked at patients who refused care after pre-hospital providers administered Narcan for a suspected opiate overdose. They then searched the death registry to see if those patients later died after refusing care (transport to the hospital).

Wampler et al. looked at 552 patients and found that no one died until at least 4 days later (1). These deaths four days later were unlikely to be from the initial overdose. A second study recently published in March of 2016 had 205 patients and showed only one death in 24 hours (2). Two others died in the 30-day follow up period which again were not likely due to the initial overdose. Combining the numbers from these two studies equates to 1/757 (0.13%) deaths.

There are limitations with all studies, but death seems unlikely after refusal of care post-narcan administration. However, our practice should not change as it relates to monitoring patients for about 4 hours to those willing. Recurrent respiratory depression is a real concern particularly seen in those patients who abuse long acting opiates. Despite this, some patients who have the capacity to make decisions may not choose the wisest care plan and may leave AMA. We must still make considerable attempts at providing substance abuse referrals and other appropriate resources as these patients are in great need of help.

There’s been a lot of chatter in the twitterverse surrounding the recent release of the POKER Trial out of Australia comparing ketofol with propofol for procedural sedation. Their primary outcomes were looking at respiratory complications, including apnea, desaturation or hypoventilation; with secondary outcomes of hypotension and patient satisfaction. They report “ketofol and propofol resulted in a similar incidence of adverse respiratory events requiring intervention by the sedating physician.” While this is true based on their data, when you start breaking down the airway interventions, propofol did require more instances of the patient requiring assisted ventilation with a BVM. Call me crazy, but to me that seems a little more of an intervention than just turning up the oxygen flow on the nasal cannula. Propofol also had a greater rate (8%) of hypotension (SBP<90) when compared to ketofol (1%), and while there were no clinically significant outcomes related to this hypotension, I think it’s still important to note. It seems like a lot of shade is being thrown (definition here) at ketofol after this trial, but I haven’t closed the door on ketofol yet. I would still give ketofol a chance, I much prefer not having to bag my shoulder reductions as the propofol wears off and while a BP of 70/40 may not stroke them out in front of you, it still gets my heart rate up a bit.

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Disclaimer: Information contained on this website is the opinion of the authors and does not represent the opinion of St. Joseph's Regional Medical Center or St. Joseph's Regional Medical Center Emergency Medicine Residency Program.